Monday, April 17, 2017

New Book: Olfactory Receptor Genes Prove Common Descent

The “Shared Error” Argument

We have seen that a new evolution book co-authored by evolutionist Dennis Venema and Scot McKnight is influenced by the mythical Warfare Thesis (here and here) and makes erroneous arguments that the fossils and echolocation support evolution (here and here). We now move on to another topic: broken genes, or pseudogenes. This is a popular argument amongst evolutionists and Venema uses as his example the olfactory receptor genes. The idea here is that, in different species (such as the human and chimpanzee), the same damaging mutation can be found in the same pseudogenes. When we find the same strange spelling mistake in the homework of different students we conclude that plagiarism occurred. It is more likely that the mistake had one source, rather than occurred twice, independently. Likewise, the same mutation in different species points to a single source in a common ancestor—common descent. Furthermore, we don’t see mutations that violate the expected pattern. Clearly common descent is the obvious, most parsimonious explanation. As Venema concludes, common descent is “overwhelmingly supported.” [36] This is a powerful argument for evolution that has influenced many people. There’s only one problem: It fails historically, philosophically, and scientifically.

First, the olfactory system is profoundly complex. Odors entering the nose interact with finely-tuned receptor proteins (created from the olfactory receptor genes), setting off an incredible cascade of events in the cell, resulting in an electrical signal sent to the brain. Studies have found that each cell expresses only a single olfactory receptor gene, and so is sensitive to a particular odor. At the brain, the signals are grouped and organized by odor. In other words, for all the cells in the nose expressing the same olfactory receptor gene (and thus sensitive to the same odor), their signals spatially converge as they feed into the brain area.

And of course, as with all the senses, These incoming signals are providing mere electrical information. There is no odor, or light, or sound entering the brain via these nerve cells. Instead, a bunch of electrical signals are entering the brain via these nerve cells. The brain, by itself, has no way of knowing what these electrical signals mean. It must somehow be given the source and meaning of these incoming signals. It then processes and interprets these signals and the end result is that we are conscious of images reported by our eyes, sounds reported by our ears, smells reported by our nose, and so forth. All of this defies evolution, and should give us pause.

Second, the evolutionist’s contention that common descent is needed to explain those shared mutations in different species contradicts the most basic biology. Simply put, similarities across species which cannot be explained by common descent, are rampant in biology. The olfactory system is no exception. Its several fundamental components, if evolution is true, must have evolved several times independently. The level of independent origin which evolutionists must admit to (variously referred to as convergent evolution, parallel evolution, recurrent evolution, cascades of convergence, and so forth depending on the pattern) is staggering and dwarfs the levels of similarities in the olfactory receptor genes. To cast those relatively few similarities as mandates for common descent, while ignoring the volumes of similarities that violate common descent constitutes the mother of all confirmation biases.

Third, the strength of this evolution argument is lack of function, but that renders it fallacious. As lawyers know, if you can’t convict the defendant on the facts, you decry how horrifying the crime is. In this case, the entire argument hinges on the utter uselessness of the broken genes. As Venema explains, they are “damaged,” “defective,” “mess[ed] up,” “wrong,” and “ruin[ed].” Clearly, according to Venema, these genes are useless—that’s why they are called pseudogenes. This is crucial because, for evolutionists, this means they would only arise by chance (what designer would implement useless designs?).

All of this means that evolutionists have a very simple formulation: Either those crippling mutations arose once in a common ancestor, or they just happened to arise by chance, coincidentally, multiple times. Clearly the former is much more likely, and this points to common descent. It is, as Venema concludes, “overwhelmingly supported.” [36]

But this powerful argument comes at a cost. There is no free lunch.

The conclusion that common descent is “overwhelmingly supported” utterly depends on our knowing the pseudogenes are useless. Disutility underwrites the assumption of chance as the only alternative to common descent. And chance as the only alternative is crucial. It is why the argument is so powerful, because the chance hypothesis is so unlikely.

Restricting the problem to a contest between evolution and chance makes evolution the obvious winner, but amidst the celebration we forget the weak link. We forget that the entire edifice resides on our certainty of disutility. This, it turns out, is a very weak link.

The history of evolutionary thought, going back to the Epicureans, is full of predictions of disutility gone wrong. It is, quite literally, a theory of gaps. When gaps in our scientific knowledge leave us with ignorance about function, evolutionists routinely assume there is no function. After all, if the world arose by chance, it should be a claptrap, full of aimless, useless designs, if they could even be called that.

But as those gaps close with the inexorable march of scientific progress, it seems we inevitably learn of function. Evolutionists are consistently claiming disutility at brand new findings, only to be proved wrong, again and again. Look no further than the seemingly endless parade of “We thought it was junk, but now …” stories.

Ultimately, the long history of disutility claims are informed by the theory rather than the evidence. This is a classic example of what philosophers refer to as theory-laden observations.

None of this means there are no truly useless structures in biology. There may well be plenty of them. But it has a terrible history.

Furthermore, regardless of the history, disutility is very difficult to know. As with the proverbial “proving a negative,” proving that a pseudogene, or anything else in biology for that matter, actually is useless, is a very difficult undertaking.

From introns to transposons, initial claims of uselessness have given way to a steady stream of findings of function. And, yes, the olfactory receptor “pseudo” genes are no exception. They are now being called pseudo-pseudogenes because all those evolutionary claims of uselessness are rapidly fading. As one recent paper concluded, “such ‘pseudo-pseudogenes’ could represent a widespread phenomenon.”

This is yet another example in a long history of failed disutility predictions. Clearly, the assumption that we know that olfactory receptor pseudogenes are useless is unfounded. Even the name (pseudogenes) will serve future generations of scientists as a constant reminder of this evolutionary foible. Venema’s powerful argument was demolished before the book was even published.

The story does not end here for even if something like pseudogenes could somehow be proven useless, this would not justify the evolutionary formulation of random chance origin as the only other alternative.

Evolution fails to explain how even a single gene could evolve, let alone the entire olfactory system. In fact the presence of supposedly useless structures, such as pseudogenes, is hardly a plus for evolution. As Elliott Sober has pointed out, there is nothing about this story that provides a positivistic argument for evolution.

The argument, and all its strength, hinges entirely on the refutation of the alternative. This is a proof by the process of elimination. Hence it becomes utterly crucial that the alternatives are carefully and exhaustively considered. In particular, all possible alternatives must be known, understood, evaluated, and disproved.

Do you see a pattern here?

This powerful evolutionary argument not only crucially depends on knowing that the pseudogenes are useless, it also crucially depends on knowing that a simple random chance model is the only alternative to evolution, for their origin.

Not only is this philosophically problematic (how do we know that the random chance model is the only alternative?), historically it has a terrible track record. As Kyle Stanford has shown, the history of science is full of theories that were advocated with this type of contrastive reasoning (by disproving a perceived alternative), only later to fail because the assumed alternative was wrong.

To summarize, this highly influential, popular, argument from similar structures that appear to be useless, lies in ruins. It is a disaster. It fails historically, philosophically, and scientifically. It should never have been used in the first place, for its scientific failure was entirely predictable from both the history and philosophy of science.

Blas: “I can´t understand how this argument is used as evidence of evolution.”

Did you not read the first first paragraph? Cornelius did a very good job explaining what the argument is and why it’s compelling at first glance. Many, many people find the argument convincing, for the reasons Cornelius pointed out. I certainly did.

”A useless gene got fixed?”

Did you not read any of the post? That’s the opposite of what the argument says: that a useful gene got broken. I think you have to be trying to misunderstand it to get it exactly backwards.

”A useless gene is conserved? Evolution should work all the other way.”

Unless a gene conveys a selective disadvantage, there is no reason it can’t persist for a very long time, even if it doesn’t do anything useful anymore. What do you mean Evolution should work the other way? Says who?

Did you not read any of the post? That’s the opposite of what the argument says: that a useful gene got broken. I think you have to be trying to misunderstand it to get it exactly backwards.

A useful gene got broken. That happened in one individual, in orther to have all the population with that gene broken the mutation should have fixed in the population. The alele with the mutation should be selected.

Unless a gene conveys a selective disadvantage, there is no reason it can’t persist for a very long time, even if it doesn’t do anything useful anymore.

Exactly what I am saying, if the GOLU gene is broken, why we yet keep it? Why the population of homo sapiens having both, the broken and the working, keeped the broken GOLU instead the functional GOLU?

Yes. [Though it would be more accurate to say ‘functional’ rather than ‘useful’. something can be functional without being useful.]

”That happened in one individual, in orther to have all the population with that gene broken the mutation should have fixed in the population.”

Yes. [assuming you mean ’in order to for the entire population to have that broken gene, it became fixed in the population.” - but that’s redundant]

”The alele with the mutation should be selected.”

No. An allele can spread throughout the population if it is neutral to survival and reproduction; it does not have to be selected for, it just can’t be strongly selected against. This is called genetic drift. This is part of population genetics, and it does’t rely on any other part of evolution being true.

Me: “Unless a gene conveys a selective disadvantage, there is no reason it can’t persist for a very long time, even if it doesn’t do anything useful anymore.”

blas: “Exactly what I am saying, if the GOLU gene is broken, why we yet keep it?”

I just explained it. There’s nothing that goes around in the genome checking to make sure genes still do something useful, and removing broken ones. If a mutation breaks a gene, but it doesn’t have a deleterious effect, it will continue to be passed down through the generations for quite some time. Through genetic drift, it may become fixed in the population, or it may die out completely.

”Why the population of homo sapiens having both, the broken and the working, keeped the broken GOLU instead the functional GOLU?

Well first, It’s not being proposed that some humans had a functional GULO gene and some had a broken one, It’s being proposed that a working GULO gene was damaged by a mutation in the common ancestor of humans and other primates who have the same damaged copy.

Second, In the instance of the GULO gene, having an inactive copy of it presumably didn’t have a serious disadvantage because the diet of most primates is rich in vitamin C. It doesn’t matter if your body can’t synthesize ascorbic acid if you eat enough of it anyway. It would be like living in Pheonix, Arizona and having a car in which the heated seats stopped working. In that climate, it’s not really a disadvantage. You may not ever even notice that it had stopped working. So essentially, the answer to why nature didn’t select for the working GULO gene over the nonworking one is that there was no selective difference between the two.

Could it be Cornelius, that the same errors or damage of genes shared among primates and human, be the result that since we share similar function and those functions are expressing those genes the most, will have a tendency to be prone to more errors due to the constant usage and that constant usage gives the appearance of common descent, but is in reality, common functions that damage the same genes over time?.I hope that was clear.in other words, same erv or pseudo gene placement is the result of similar functions being expressed at the same loci, and its the similar functions that give rise to the same damaged areas?.

bmk777k: “Could it be Cornelius, that the same errors or damage of genes shared among primates and human, be the result that since we share similar function and those functions are expressing those genes the most, will have a tendency to be prone to more errors due to the constant usage and that constant usage gives the appearance of common descent, but is in reality, common functions that damage the same genes over time?”

Short answer: Nope.

Long answer: Noooooope.

To borrow from a common meme, that’s not how this works; that’s now how any of this works. If you crack the lens on your phone, it doesn’t corrupt the camera driver. If you burn the cake in the oven, it doesn’t scramble the recipe. Cornelius probably won’t point out the misunderstanding of the relationship between genotype and phenotype at the root of your question, because he usually doesn’t correct ‘his team’ on scientific or logical errors.

“…due to the constant usage and that constant usage gives the appearance of common descent, but is in reality, common functions that damage the same genes over time?”

See Blas, here’s someone else who sees how shared pseudogenes do actually give the appearance of common descent.

bmk777k, the interesting thing is that you’re not the only creationist I’ve heard propose this as a solution to the pseudogene ‘problem’ when learning about it for the first time. I think even creationists see that it does strongly imply common ancestry, unless they can think of an alternate explanation; to use Cornelius’ example, an alternate explanation for how both students wound up with the same odd spelling error. Unfortunately, there aren’t really any and Cornelius knows this, so his only recourse is to try to convince people that it isn’t actually a compelling argument for common ancestry in the first place.

”…in other words, same erv or pseudo gene placement is the result of similar functions being expressed at the same loci, and its the similar functions that give rise to the same damaged areas?”

You’re on the right track in that you seem to realize that unless there’s another plausible reason that the genes should break in the same place, it leaves common ancestry as the most parsimonious explanation. If you continue your research, you’ll find that there aren’t really any currently known mechanisms that are more plausible, so Cornelius is trying to head you off at the pass by assuring you that you don’t need to actually look for alternate explanations, that you were incorrect to see shared pseudogenes as an indicator of common ancestry in the first place. (pay no attention to the pseudogenes behind the curtain.)

I agree with the poster bmk777k or like that.This was a great thread to show how evolution of such genes is unlikely.Yet to offer a reason as to why the same error WHY NOT just like bodies would likely have like problems/errors for some good reason in dealing in nature.?!Its not demanding to see common descent from a simple like detail.Our body with apes is identical and so why not identical reactions?!

Cornelius, I take it that you don’t believe in paternity tests? Wouldn’t the argument for relatedness made by that methodology fail for the same reason?

Are you suggesting that there are no such things as pseudogenes? That GULO is … functional? For there to be no pseudogenes, it would have to be the case that a mutation (or millions of mutations) can’t break a gene’s function. Surely you’re not claiming that? Or are you just claiming that we can’t ‘know’ a gene is no longer functional for the same reason we can’t ‘know’ that mermaids don’t exist?

Are you suggesting that there are no such things as pseudogenes? That GULO is … functional? For there to be no pseudogenes, it would have to be the case that a mutation (or millions of mutations) can’t break a gene’s function. Surely you’re not claiming that?

That almost qualifies as an own-goal, which would be 2 more points against evolution. From the OP:

Cornelius “That almost qualifies as an own-goal, which would be 2 more points against evolution. From the OP: None of this means there are no truly useless structures in biology.”

Let me get this straight: You think that when an ‘evolutionist’ misses a sentence in a blog post, that’s a ‘point’ against the theory of evolution? You could be saying that partially in jest, but it’s hard to tell since many of your other arguments against evolution have the same level of cogency. But… did I actually miss that sentence?

“From the OP: None of this means there are no truly useless structures in biology.”

You said structures; I asked about pseudogenes. Presumably you could believe that there are some useless structures in biology, but that pseudogenes aren’t counted among them. You clearly state your skepticism of the of disutility of pseudogenes in several places…

“Furthermore, regardless of the history, disutility is very difficult to know. As with the proverbial “proving a negative,” proving that a pseudogene, or anything else in biology for that matter, actually is useless, is a very difficult undertaking.

“Clearly, the assumption that we know that olfactory receptor pseudogenes are useless is unfounded.”

…and you never acknowledge that you think that any genes are actually nonfunctional. In fact, you strongly imply that you think that they’re not:

”Even the name (pseudogenes) will serve future generations of scientists as a constant reminder of this evolutionary foible.” (emphasis mine)

It sounds like you’re not just saying that some pseudogenes will have a function discovered in the future, but rather that the whole concept of a ‘pseudogene’ will be seen by future generations as erroneous. (otherwise, why would those future generations see anything wrong with the concept of pseudogenes, even if there were slightly fewer than once thought?)

My mistake was breaking a single question over two sentences, as you only responded to the first part of it without answering the question itself. So I’ll rephrase for clarity:

1. Are you suggesting that there are no such things as pseudogenes, or are you just claiming that we can’t ‘know’ a gene is no longer functional, in the same way that we can’t ‘know’ that mermaids don’t exist? (Hard to prove a negative, as you say) (As an addendum, 1b: Can we know for sure what a specific gene’s function is? I.e, if a certain gene provided the ability to synthesize ascorbic acid, would we have a way to know that, with a reasonable degree of certainty? Would we be able to infer the that same gene, if found in another individual of the same species, did the same thing even if we couldn’t observe it being expressed in the second case?

Are you suggesting that there are no such things as pseudogenes, or are you just claiming that we can’t ‘know’ a gene is no longer functional, in the same way that we can’t ‘know’ that mermaids don’t exist? (Hard to prove a negative, as you say)

Neither, but it is difficult to prove no function. That is in contrast to our level of knowledge. IOW, it is not as though we have fairly compelling evidence for non function, the only thing stopping us from the obvious conclusion is a philosophical technicality. You are not seeing this because you are seeing the evidence through evolutionary lenses. IOW, the evidence is theory-laden, and therefore it is interpreted as fairly compelling evidence for non function. Pretty much a no-brainer. But from a theory-neutral perspective this is not the case. If you cannot see this, then at least look at the history of your argument.

(As an addendum, 1b: Can we know for sure what a specific gene’s function is? I.e, if a certain gene provided the ability to synthesize ascorbic acid, would we have a way to know that, with a reasonable degree of certainty? Would we be able to infer the that same gene, if found in another individual of the same species, did the same thing even if we couldn’t observe it being expressed in the second case?